1Microbes and diseases: what to study-1

• 1. Causative microbe: name, morphology (shape, size, Gram stain, etc.), physiology (aerobe, anaerobe, etc) and some info on classification (what's it related to?)

• 2. Pathogenesis and clinical disease:  what disease does it cause (signs and symptoms) and how does it do it (capsule, toxins..)?

• 3. Transmission and epidemiology: how do you get the disease?

2Microbes and diseases: what to study-2

• 4. Diagnosis: How does the lab usually identify the causative agent?

• 5. Treatment: antibiotics prescribed (or not- no cell wall, no penicillin) or other treatment (oral rehydration therapy for cholera).

• 6. Prevention and control (stop the spread; condoms, kill urban rats..)

3Pathogenic Bacteria

• Gram positive rods and cocci– Pyogenic cocci: Staph and Strep– Gram positive rods: Bacillus to Actinomycetes

• Gram negative cocci and bacilli– Gram negative cocci: Neisseria– The Enteric bacteria– Aerobic & Anaerobic Gram negative bacteria

• Miscellaneous pathogens– Mycoplasmas to Helicobacter; Gram -, but odd

4Staphylococcus: G+ coccus

• S. aureus and S. epidermidis.– S. aureus much worse, S. epi an opportunist.– Sturdy, salt tolerant, fac anaerobes; clusters– S. epidermidis common on skin, S. aureus less.

• Diseases of S. aureus– Food poisoning, skin diseases (impetigo, folliculitis,

furuncles & carbuncles, scalded skin syndrome), systemic diseases (TSS, bacteremia, heart, lung, and bone infections)

– Diseases spread by fomites and direct contact.

5S. aureus virulence factors & Rx

• Coagulase, triggers blood clotting.• Capsules, hyaluronidase, staphylokinase, beta-

lactamases (destroy penicillins)• Toxins: various, including TSS toxin, exfoliatin,

and enterotoxins (heat stable)• 95% resistant to penicillin, but now many

resistant to methicillin, and now vancomycin leaving ??

6Streptococci: G+ cocci

• Genera: Steptococcus and Enterococcus• Aerotolerant anaerobes, catalase negative

– Grow in chains, pairs– Strep: Lancefield groups, viridans, S. pneumoniae

• Group A strep: S. pyogenes– Pharyngitis, scarlet fever, pyoderma, erysipelas,

TSS, necrotizing fasciitis– Sequelae: rheumatic fever and glomerulonephritis

• Group B strep: S. agalactiae– Infects newborns during birth, various illnesses

7Virulence factors, etc.

• S. pyogenes (“pus-producing”)– M protein and capsule: avoids phagocytosis– Streptokinase, streptolysins for escape & attack– Pyrogenic erythrotoxins (SPEs) 3 different types

• Cause scarlet fever: fever, rash– Beta hemolytic on blood agar

• Viridans group: greenish alpha hemolysis– Common in throat, mouth, but can be opportunists– S. mutans associated w/ dental caries

8S. pneumoniae

• Gram + coccus in pairs, alpha hemolytic• Pneumonia, sinusitis, otitis media, meningitis• Major virulence factor is a capsule

– Other unrelated bacteria also have capsules, cause meningitis

– Also, get phagocytized by “non-professionals”, spread

• Carried in URT by 75% of population– Disease greatest in children and elderly

9Enterococcus

• Formerly part of Group D Strep• Grow under conditions (e.g. high salt) that

Strep do not tolerate.• E. faecium, E. faecalis found in GI tract• Opportunists

– Cause of nosocomial, wound infections• Resistant to most antibiotics

– Plasmids transfer resistance to others

10Bacillus: G+ rods-1

• Bacillus species very common and numerous– Present in soil, most non-pathogenic– All form endospores when nutrient limited

• Bacillus cereus: cause of GI distress– Emetic and diarrheal toxins; bad rice

http://biochem.ultraevil.com/bio/Images/bioloskoorozje/anthrax/BacillusAnthrax.jpg

11Bacillus: G+ rods-2

• Bacillus anthracis: cause of anthrax– Anti-phagocytic capsule of glutamic acid– 3 protein toxin that is lethal– Zoonotic: primarily disease of livestock– Ingestion, inhalation, and cutaneous forms

• Black eschar characteristic of cutaneous form– Not hemolytic; antibiotics, vaccine effective

12Clostridium: G+ rods• Strict anaerobes! Endospore formers. Toxigenic

– Common in soil, sewage animal GI tracts– Produce neurotoxins, enterotoxins, histolytic toxins

• Four important species: C. perfringens, C. botulinum, C. tetani, and C. difficile.

• C. perfringens– Food poisoning: cramps and diarrhea– From injury: myonecrosis to gas gangrene

• Fermentation in tissues, killing of tissues and spread of cells into anaerobic areas.

• Oxygen treatment, debridement, amputation

13More clostridia• C. difficile: normal GI microbiota

– Cause of pseudomembranous colitis, resulting from overgrowth following broad spectrum anitbiotics• Damage to GI wall can lead to serious illness

– Nosocomial infection, easily transmitted• C.botulinum: cause of botulism

– Usually acquired by ingestion: intoxication• Food borne, infant (no honey), wound

– Produces neurotoxin, inhibits acetylcholine release• Flaccid paralysis; Botox: deadly poison / beauty

– Mouse bioassay; administer antitoxin

14More clostridia-2

• C. tetani: cause of tetanus– Growth in anaerobic wounds, makes tetanus toxin– Toxin prevents action of inhibitory neurons

• Opposing muscle pairs both contract• Spastic paralysis, leading to death.

– Recommendation is booster shot every 10 years• Toxoid vaccine, with diphtheria toxin• No natural immunity: you die first.

15Listeria: Gram + rod• L. monocytogenes, non-spore forming

coccobacillus– Common in many environments

• Portal of entry is food or drink–Esp. meat, dairy products. Check for recalls.–Is psychrotrophic.

– Escapes into cytoplasm during phagocytosis• Lives intracellularly, moves cell to cell

– Severe infections in: pregnant women/fetuses, newborns, elderly, immunocompromised

16Corynebacterium: G+ rod

• Found on humans, animals, plants– Normal microbiota and opportunists

• C. diphtheriae: cause of disease diphtheria– Colonizes the throat, inflammation, fever, and

pseudomembrane, release of toxin• Pseudomembrane can block throat

– Toxin inhibits protein synthesis, kills cells locally• Toxin diffuses, kills heart and nerve cells

– Antitoxin, antibiotic treatment– Vaccination (DPT); humans are only host.

17Mycobacterium: G+ rods• Many non-pathogenic species, most disease:

M. tuberculosis and M. leprae– M. avium-intracellulare: environmental source of

lung disease (like TB) in AIDS patients– Mycolic acids as part of complex cell wall

• Protects against dessication• Protects against destruction by phagocytes• Requires acid-fast staining

– Generally grow very slowly (chronic illnesses)– Can grow intracellularly

18M. tuberculosis

• Causes disease tuberculosis, mostly lung dis.• Cord factor: cell wall factor that connects cells,

resists phagocytosis, toxic to host cells• Disease: cells enter lungs, infect macrophages

– Cell mediated immunity fights back, walls off infection; forms tubercle (caseous necrosis occurs)

– Disease remains controlled, cured, or returns• Disseminated TB: spreads thru body

• Worldwide problem; lowered immunity=risk– Skin test, chest x-ray, drug treatment, vaccine?

19M. leprae

• Cause of Hansen’s disease, aka leprosy• Slow growing, likes it cool; armadillos as model• Grows in peripheral nerve and skin cells

– Numbness is characteristic of disease• Tuberculoid vs. lepromatous leprosy

– Mild, severe, respectively, depending on cell mediated immune response.

– Numbness vs tissue destruction• Spread mostly by direct contact• Treatable with antibiotics, but long term

20Other Gram positive rods

• Propionibacterium – Ferments, produces propionic acid and CO2

– makes Swiss cheese– P. acnes: causes inflammation of sebaceous

glands: acne. Bacterial growth stimulated by excessive oil production.

• Diphtheroids– Bacteria resembling Corynebacterium diphtheriae

as normal microbiota on skin.

21Other G+ -2

• Partially to totally filamentous bacteria– Nocardia asteroides

• Causes skin and lung disease• Filamentous cells with pus, draining• Acid fast

– Actinomycetes• Large group of filamentous bacteria• Mostly environmental, source of geosmin,

antibiotics• Some species do cause infections

–abscesses